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1.
背景:嗅鞘细胞移植和甲基强的松龙是两种非常有前途的治疗脊髓损伤方法,关于二者联合治疗脊髓损伤的报道较少,结果也不尽相同。 目的:通过对大鼠行为学评分和诱发电位学检测了解嗅球嗅鞘细胞移植和甲基强的松龙对大鼠急性脊髓损伤的修复作用以及二者之间有无协同作用。 方法:以NYU脊髓打击法建立大鼠急性T10脊髓损伤模型,术后分别注射嗅鞘细胞、甲基强的松龙、嗅鞘细胞+甲基强的松龙、无血清的DF12培养液、生理盐水。于术后8周进行后肢体感诱发电位、运动诱发电位检测,并通过BBB评分了解各组大鼠手术前、后运动功能的变化。 结果与结论:术后8周,嗅鞘细胞组、甲基强的松龙组、嗅鞘细胞+甲基强的松龙组与损伤组、DF12组比较,大鼠后肢BBB评分明显升高,体感诱发电位、运动诱发电位 N1波潜伏期缩短,波幅升高,差异有显著性意义(P < 0.05)。嗅鞘细胞+甲基强的松龙组与嗅鞘细胞组、甲基强的松龙组比较,大鼠后肢BBB评分明显升高,体感诱发电位、运动诱发电位N1波潜伏期缩短,波幅升高,差异有显著性意义(P < 0.05)。说明嗅鞘细胞移植和甲基强的松龙单独应用均可以显著促进急性脊髓损伤大鼠运动功能恢复。二者联合促进急性脊髓损伤大鼠运动功能恢复的效果更加显著。  相似文献   

2.
背景:建立有效的完全性脊髓损伤动物模型是深入研究脊髓损伤的前提,只有建立标准的、可重复性高的实验动物模型才能择优选出治疗脊髓损伤的可行方案。 目的:实验拟建立一种稳定的大鼠完全性脊髓损伤动物模型。 设计、时间及地点:对照观察动物实验,于2007-11/2008-10在石河子大学药学院动物试验中心完成。 材料:30只健康Wistar大鼠随机分成假手术组6只、实验组24只。 方法:显露实验组大鼠T8~T12棘突及椎板,切除T9~10棘突及椎板,暴露相应脊髓段作为损伤区,采用大鼠脑定位仪自主设计改良Allen模型打击装置,予15 g×20 cm=2.94×10-2N 重力打击大鼠T10节段脊髓,动物模型保证硬脊膜完整。假手术组仅同法暴露相应脊髓段,但不做打击。 主要观察指标:造模后2,4,8周以斜板试验及BBB评分观察大鼠双后肢运动功能,以苏木精-伊红染色观察大鼠脊髓组织的变化。 结果:假手术组大鼠苏醒后能站立行走,斜板试验角度均大于70°,BBB评分21分,脊髓结构正常。实验组大鼠造模后双下肢全瘫,2只大鼠表现为痉挛性瘫痪,5只大鼠表现出不同程度的自残现象。造模后2,4,8周斜板试验角度均小于30°,BBB评分均少于10分,随时间延长,部分大鼠可见后肢刺激性反射,但无主动性功能活动,局部脊髓结构破坏严重。 结论:以2.94×10-2N 重力打击大鼠脊髓可保证硬脊膜的完整,并获得稳定的完全性脊髓损伤动物模型。  相似文献   

3.
甲基强的松龙和神经干细胞移植联合治疗大鼠脊髓损伤   总被引:6,自引:1,他引:5  
目的:观察甲基强的松龙和神经干细胞移植对大鼠脊髓损伤后神经结构修复和功能恢复的治疗作用并探讨其作用机制。方法:制备大鼠胸10脊髓损伤模型,体外培养、诱导分化大鼠神经干细胞,定量评价甲基强的松龙和神经干细胞移植对脊髓损伤后神经结构修复和功能恢复的影响。结果:与对照组相比,移植组明显地增强了生长相关蛋白(GAP-43)mRNA的表达,促进了乙酰胆碱转移酶(ChAT)阳性脊髓运动神经元的再生、神经结构的修复和下肢运动功能的恢复(P<0.05)。结论:甲基强的松龙和神经干细胞移植通过增强GAP-43 mRNA的表达、运动神经元的再生而促进了脊髓损伤后神经结构的修复和功能的恢复,是急性脊髓损伤的一种有效的治疗方案。  相似文献   

4.
目的:促红细胞生成素为肾源性细胞因子,在大鼠急性脊髓损伤后对脊髓神经功能具有保护作用。实验拟证明不同时间硬膜外腔注射后其对脊髓神经细胞凋亡的影响。 方法:实验于2007-01/04在苏州大学附属第二医院动物实验室完成。①实验材料:清洁级成年雄性SD大鼠48只,体质量(270 ±10) g;实验用人重组促红细胞生成素为日本麒麟啤酒株式会社制造,规格3 000 IU /支。②实验分组及处理:将大鼠随机分为正常组6只,假手术组6只(仅切除椎板),生理盐水组18只,实验组18只。按改良Allen打击法建立大鼠脊髓不完全损伤模型。实验组分别于大鼠脊髓损伤后1,6,24 h(每个时间点6只),于硬膜外腔注射重组人促红细胞生成素5 000 u/(kg?bw);生理盐水组于相同时间予以相同体积生理盐水。③实验评估:通过动物神经运动功能BBB评分及斜板试验评价神经损伤程度;苏木精-伊红染色法观察组织学改变,并采用原位末端标记法标记法检测脊髓神经细胞凋亡数。 结果:①神经行为学评分:正常组、假手术组大鼠双下肢运动功能正常;与生理盐水组相比,脊髓损伤后实验组1,6及24 h神经运动功能有改善;斜板角度及BBB评分均明显提高,差别有显著性意义(P < 0.05)。②组织学苏木精-伊红染色结果:实验组组织学破坏改变明显较生理盐水组轻。③凋亡神经细胞及计数结果:实验组脊髓神经细胞凋亡指数均明显下降,差异有显著性(P < 0.05)。 结论:早期应用外源性促红细胞生成素对脊髓不完全损伤后引起的神经运动功能损害具有保护作用,能明显改善脊髓损伤后的临床功能表现。此种保护作用与促红细胞生成素能够抑制神经细胞凋亡有关。  相似文献   

5.
观察汉防己甲素(Tetrandrine ,Tet)对大鼠急性脊髓损伤后组织结构神经细胞凋亡和运动功能恢复的影响并探讨其作用机制。方法:选用100只成年大鼠,随机分为四组,即假手术组10只(A组)、损伤对照组(B组)30只、甲基强的松龙治疗组(CD组)30只、Tet治疗组(DC组)30只。胸8、9椎板切除后B、C、D组用加速压迫型Allen’s打击法制成脊髓损伤模型。C组和D组动物于制模前、伤后24h、伤后48h尾静脉注射甲基强的松龙(MP)和Tet。各组大鼠于术后8h,1d,3d,7d,14d行BBB评分,分别于术后8h,1d,3d,7d,14d取损伤段脊髓行石蜡切片HE染色,观察脊髓组织的形态结构变化和免疫组织化学染色检测细胞凋亡因子bcl-2、bax 。结果: 伤后7d、14dC组与D组大鼠运动功能评分(BBB评分)显著高于B组,各时间点C组与D组评分无统计学意义;A组的脊髓组织HE染色正常 ,C组与D组脊髓组织损害较B组轻,术后8h-14d动态观擦,3d—7d损伤表现最为严重,达到损伤高峰期;A组中bax、bcl-2表达较少,C组与D组bax 表达较B组少,而bcl-2表达较B组多。结论:汉防己甲素可通过增加bcl-2表达、降低bax 表达,抑制急性脊髓损伤后神经细胞的凋亡,能有益于脊髓组织的保护,促进运动功能的恢复。  相似文献   

6.
目的 探讨甲基强的松龙(methylprednisolone,Meth)对大鼠脊髓损伤(spinal cord injury, SCI)后神经细胞凋亡及wnt/β-catenin信号通路的影响。方法 将60只SD成年大鼠随机分为3组,即假手术(Sham)组、甲基强的松龙(Meth)组和生理盐水(Saline)组,每组各20只;假手术组仅需切开椎板不损伤脊髓,甲基强的松龙组和生理盐水组采用改良Allens法制作大鼠脊髓损伤模型后立即从尾静脉注射大剂量MP治疗,并在术后第1、2 d相同的时间点分别注射1次;采用尼氏染色(Nissl)观察组织形态变化;采用免疫荧光观察蛋白caspase-3表达水平;采用Western Blot检测各组wnt/β-catenin信号通路蛋白GSK-3β和β-catenin的表达水平。结果 甲强的松龙组(Meth)第7 d SCI较生理盐水组明显减轻(P0.01);Meth组抑制凋亡蛋白caspase-3表达水平明显下调(P0.01);大鼠急性脊髓损伤(SCI)后第3、7 d,甲基强的松龙组呈现抑制蛋白GSK-3β表达(P0.05),而蛋白β-catenin表达则明显上调(P0.05)。结论 大鼠急性脊髓损伤后MP可能通过激活wnt/β-catenin信号通路来促进大鼠运动功能恢复以及抑制急性脊髓损伤神经细胞的凋亡。  相似文献   

7.
目的研究减重平板训练联合应用大剂量甲基强的松龙(MP)对脊髓损伤大鼠运动功能恢复的影响。方法成年雄性SD大鼠48只,随机分为正常对照组(A组)、损伤对照组(B组)、单纯平板组(C组)、联合治疗组(D组)各12只。采用改良Allen's撞击法制作T10不完全性脊髓损伤模型。C组损伤后1周开始平板训练,30min/d,每周5d,共4周,D组于损伤后24h内给予大剂量甲基强的松龙琥珀酸钠冲击治疗,1周后平板训练,30min/d,每周5d,共4周。B组损伤后不作处理。分别在损伤前、损伤后1周、2周、3周、4周和5周时采用斜板试验、改良Tarlov评分、BBB评分进行运动功能评定。结果(1)损伤后第1周,联合治疗组运动功能评分高于损伤对照组和单纯平板组(但P0.05)。(2)训练2周后开始,联合治疗组运动功能评分明显高于单纯平板组和损伤对照组,且单纯平板组也显著高于损伤对照组(P0.05)。结论减重平板训练可促进SCI大鼠运动功能的恢复,且减重平板联合甲基强的松龙比较单纯平板训练更能促进SCI大鼠运动功能的恢复。  相似文献   

8.
背景:目前研究多为骨髓间充质干细胞的体外培养及细胞移植对颅内疾病的治疗,对植入细胞在损伤脊髓中的成活、分化、迁移、结构重建等了解有限。 目的:探讨局部骨髓间充质干细胞移植在脊髓损伤修复中的作用和骨髓间充质干细胞替代治疗的可行性。 方法:成年健康雌性SD大鼠随机分为细胞移植组和对照组,建立SD大鼠脊髓横断损伤模型,伤后即刻分别向损伤区局部移植大鼠骨髓间充质干细胞悬液或无钙镁磷酸缓冲液。在术前和术后1 d,1周,2周,3周,4周和8周进行BBB评分,观测大鼠的运动功能,并于移植后1周免疫组织化学染色法观察BrdU标记的骨髓间充质干细胞在脊髓损伤处的存活情况,移植后4周进行损伤脊髓的大体观察和组织学检测。 结果与结论:移植后第1~8周细胞移植组BBB评分均髙于对照组;术后1周免疫组织化学染色结果显示在细胞移植组大鼠脊髓远端检测到BrdU阳性细胞,术后4周脊髓损伤处发现有神经纤维。证实通过损伤后立即局部注射的方式将骨髓间充质干细胞移植进大鼠脊髓损伤区,细胞可在损伤区存活;存活的骨髓间充质干细胞可分化为神经元,在损伤局部形成神经元通路,从而促进脊髓神经纤维传导功能的恢复,并促进高位脊髓损伤后大鼠后肢运动功能恢复。  相似文献   

9.
背景:研究证实脂肪间充质干细胞在体外经丹参等诱导剂诱导后可分化为神经元样细胞,因此有可能成为治疗脊髓损伤新的种子细胞。 目的:探讨脂肪间充质干细胞尾静脉移植后,对急性闭合性脊髓损伤大鼠行为学及损伤脊髓组织中各因子表达的影响。 方法:无菌条件下体外分离培养人脂肪间充质干细胞,传至第4代,将细胞收集并制成浓度为1×109 L-1细胞悬液。盐水对照组、细胞移植组大鼠建立脊髓损伤模型,造模成功后1周,细胞移植组经尾静脉注射1 mL干细胞悬液,盐水对照组同法注射等体积的生理盐水,模型对照组不做任何处理。 结果与结论:与模型对照组和盐水对照组比较,细胞移植组大鼠后肢运动功能明显恢复,BBB评分明显升高(P < 0.05);胶质纤维酸性蛋白阳性表达明显减少(P < 0.05),神经元特异性烯醇化酶、巢蛋白的阳性表达均明显升高(P < 0.05)。移植后3 d及1周,在损伤区及临近的脊髓节段可见经荧光染料标记的脂肪间充质干细胞,主要聚集在受损伤脊髓节段1 cm范围内,呈不均匀分布。提示急性闭合性脊髓损伤大鼠经尾静脉移植人脂肪间充质干细胞后,其行为学得到改善,受损脊髓节段局部神经元细胞分化明显增多,修复速度加快。  相似文献   

10.
移植人脐带间充质干细胞修复大鼠脊髓损伤   总被引:1,自引:0,他引:1  
背景:已知人脐带间充质干细胞对脊髓损伤存在着潜在的治疗价值,然而,当前对移植人脐带间充质干细胞治疗脊髓损伤及机制方面研究很少。 目的:观察人脐带间充质干细胞对脊髓损伤大鼠的治疗效果。 方法:40只Wistar大鼠建立脊髓损伤模型,38只造模成功后随机摸球法分为3组:空白对照组:只接受单纯损伤,不做任何移植;DMEM移植组:损伤后1周予以5 μL DMEM局部移植;细胞移植组:损伤后1周予以5 μL准备好的人脐带间充质干细胞局部移植(细胞数1×106)。移植后对实验动物通过BBB评分、体感诱发电位与运动诱发电位观察后肢功能恢复情况。分别于损伤后2,4,6,8,10周随机于细胞移植组抽取大鼠2只,免疫组织化学染色观察人脐带间充质干细胞存活、迁移、分化,通过胶质纤维酸性蛋白阳性细胞染色比较各组损伤局部胶质瘢痕形成面积。 结果与结论:BBB评分损伤后4周细胞移植组高于其他两组(P < 0.05),损伤后12周细胞移植组与其他两组相比SEP、MEP潜伏期缩短、波幅值增高(P < 0.05)。免疫组织化学染色示人脐带间充质干细胞可向神经元、星形胶质细胞和少突胶质细胞分化,分化的少突胶质细胞并包绕轴突形成髓鞘。细胞移植组损伤局部胶质瘢痕面积均小于其他两组(P < 0.05),空白对照组、DMEM移植组间差异无显著性(P > 0.05)。提示未经体外诱导的人脐带间充质干细胞可于损伤大鼠脊髓体内向神经元、星形胶质细胞、少突胶质细胞分化,减小胶质瘢痕,并促进脊髓损伤大鼠神经功能的恢复。  相似文献   

11.
Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.  相似文献   

12.
Diagnostic Difficulties and Treatment Implications   总被引:1,自引:0,他引:1  
Robert J. Gumnit 《Epilepsia》1987,28(S3):S9-S13
Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.  相似文献   

13.
Cognitive Dysfunction Associated with Antiepileptic Drug Therapy   总被引:7,自引:5,他引:2  
Eileen P.G. Vining 《Epilepsia》1987,28(S2):S18-S22
Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.  相似文献   

14.
B. J. Wilder 《Epilepsia》1987,28(S2):S1-S7
Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.  相似文献   

15.
Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.  相似文献   

16.
Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.  相似文献   

17.
Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity   总被引:5,自引:1,他引:4  
G. Trube  R. Netzer 《Epilepsia》1994,35(S5):S62-S67
Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.  相似文献   

18.
Hepatic Considerations in the Use of Antiepileptic Drugs   总被引:5,自引:4,他引:1  
Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.  相似文献   

19.
Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.  相似文献   

20.
Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.  相似文献   

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